Researchers at Memorial Sloan-Kettering Cancer Center in New York found detectable proximal muscle weakness in nine out of 15 adult patients receiving adrenocorticosteroids for cancer. The study authors determined that weakness was significantly related to the cumulative dose of steroid administered, and that the weakness improved or resolved in the three patients who were removed from steroid therapy. In 1985, researchers found hip flexor weakness (compared to age- and sex-matched controls) in 64 percent of patients taking 40 mg of prednisone or more per day for asthma relief. Betty and Elyn represent good examples of the two types of myopathy that can result from elevated levels of steroid administration. Betty’s case is more consistent with chronic (classical) steroid myopathy, which John Wald, MD, called the most common medication-induced muscle disorder at the annual assembly of the American Academy of Physical Medicine and Rehabilitation in Orlando last year. Wald reported that up to 60 percent of patients may see its effects, depending upon dose and duration of steroid administration. Chronic myopathy presents as a slowly progressive, painless weakness, and can include weakness of the diaphragm in addition to the proximal limbs (especially after using inhaled steroids), Dr. Onset is often subtle, occurring months to years after initiation of steroid therapy, though it can be seen in less than two weeks. Elyn, on the other hand, experienced acute myopathy, which occurs after short-term treatment with high doses of steroids, generally greater than 20 mg/day. Some degree of painless proximal weakness, usually symmetrical, develops over days with this form, what steroids do not convert to dht. Because of its possible effect on the diaphragm, acute steroid myopathy is of particular concern in acute care units and ICUs. Acute weakness after only five days of methylprednisolone at 60 mg/day has been reported, though incidence is higher with a cumulative dose of greater than 5 grams of hydrocortisone, Dr. Nutritional deficiencies, sepsis and underlying neuropathies make a patient more vulnerable. The Role of Exercise. The only proven way to resolve the symptoms of steroid-induced myopathy is to stop taking them. Most of it is focused on exercise. While no special rehabilitation program for steroid-induced myopathy has yet been tested in human beings, 5 animal studies show promise. Japanese researchers studying muscle response in rats concluded that even mild aerobic exercise can prevent the onset of steroid myopathy. After four weeks, areas of type I fibers in the soleus and type IIa fibers in the digitorum longus muscle were found to be significantly larger in the steroid-plus-exercise group than the steroid alone group. Although the proportion of type I fibers in the soleus was significantly lower in the steroid alone rats than in the other three groups, there was little difference in fiber type distribution between the steroid-plus-exercise group and the control. Initial research findings also bode well for the benefits of resistance exercise. For one, resistance exercise carries bone-building properties that can inhibit bone loss, which often correlates with steroid myopathy. And a study out of the University of Florida’s College of Health and Human Performance found that heart transplant recipients responded favorably to resistance exercise as part of a strategy to prevent steroid-induced myopathy. Fourteen male heart transplant recipients were split into a control group and one that trained with lumbar extension and variable resistance Nautilus exercises one to two days per week. Six months of such training restored fat-free mass to pre-transplant levels and higher in the exercise group, while the control group showed a progressive decline in fat-free mass during the same period.
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